Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

Glaucoma

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 57

Glaucoma

From Wikipedia, the free encyclopedia

Glaucoma

Acute angle closure glaucoma of the person's right eye (shown at left).

Note the mid-sized pupil, which was non-reactive to light, and redness

of the white part of the eye.

Specialty Ophthalmology

Symptoms Vision loss, eye pain, mid-dilated pupil, redness of

the eye, nausea[1][2]

Usual onset Gradual, or sudden[2]

Risk factors Increased pressure in the eye, family

history, migraines, high blood pressure, obesity[1]

Diagnostic Dilated eye examination[1]

method

Similar Uveitis, trauma, keratitis, conjunctivitis[3]

conditions

Treatment Medication, laser, surgery[1]

Frequency 6–67 million[2][4]

[edit on Wikidata]
Glaucoma is a group of eye diseases which result in damage to the optic nerve and vision loss.
[1]
 The most common type is open-angle glaucoma with less common types including closed-angle
glaucoma and normal-tension glaucoma.[1] Open-angle glaucoma develops slowly over time and
there is no pain.[1] Side vision may begin to decrease followed by central vision resulting
in blindness if not treated.[1] Closed-angle glaucoma can present gradually or suddenly. [2] The sudden
presentation may involve severe eye pain, blurred vision, mid-dilated pupil, redness of the eye, and
nausea.[1][2] Vision loss from glaucoma, once it has occurred, is permanent. [1]
Risk factors for glaucoma include increased pressure in the eye, a family history of the
condition, migraines, high blood pressure, and obesity.[1] For eye pressures a value of greater than
21 mmHg or 2.8 kPa is often used with higher pressures leading to a greater risk.[2][5] However, some
may have high eye pressure for years and never develop damage. [2] Conversely, optic nerve damage
may occur with normal pressure, known as normal-tension glaucoma. [6] The mechanism of open-
angle glaucoma is believed to be slow exit of aqueous humor through the trabecular meshwork while
in closed-angle glaucoma the iris blocks the trabecular meshwork.[2] Diagnosis is by a dilated eye
examination.[1] Often the optic nerve shows an abnormal amount of cupping.[2]
If treated early it is possible to slow or stop the progression of disease with
medication, laser treatment, or surgery.[1] The goal of these treatments is to decrease eye pressure.
[2]
 A number of different classes of glaucoma medication are available.[2] Laser treatments may be
effective in both open-angle and closed-angle glaucoma. [2] A number of types of glaucoma
surgeries may be used in people who do not respond sufficiently to other measures. [2] Treatment of
closed-angle glaucoma is a medical emergency.[1]
About 6 to 67 million people have glaucoma globally. [2][4] The disease affects about 2 million people in
the United States.[2] It occurs more commonly among older people. [1] Closed-angle glaucoma is more
common in women.[2] Glaucoma has been called the "silent thief of sight" because the loss of vision
usually occurs slowly over a long period of time.[7] Worldwide, glaucoma is the second-leading cause
of blindness after cataracts.[2][8] The word "glaucoma" is from ancient Greek glaukos which means
blue, green, or gray.[9] In English, the word was used as early as 1587 but did not become commonly
used until after 1850, when the development of the ophthalmoscope allowed people to see the optic
nerve damage.[10]

Video explanation

Contents
  [hide] 

 1Signs and symptoms


 2Causes
o 2.1Dietary
o 2.2Ethnicity
o 2.3Genetics
o 2.4Other
 3Pathophysiology
 4Diagnosis
o 4.1Primary glaucoma and its variants
o 4.2Developmental glaucoma
o 4.3Secondary glaucoma
o 4.4Absolute glaucoma
o 4.5Types
 5Screening
 6Treatment
o 6.1Medication
o 6.2Laser
o 6.3Surgery
 7Prognosis
 8Epidemiology
 9History
o 9.1Etymology
 10Research
o 10.1Rho kinase inhibitors
o 10.2Neuroprotective agents
o 10.3Cannabis
 11References
 12External links

Signs and symptoms[edit]

Photo showing conjunctival vessels dilated at the corneal edge (ciliary flush, circumcorneal flush) and hazy
cornea characteristic of acute angle closure glaucoma

Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms
make screening via regular eye check-ups important. The only signs are gradually progressive visual
field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).
About 10% of people with closed angles present with acute angle closure characterized by sudden
ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg), nausea
and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an
oval pupil in some cases. Acute angle closure is an emergency.
Opaque specks may may occur in the lens in glaucoma, known as glaukomflecken. [11]
Causes[edit]

A normal range of vision

The same view with advanced vision loss from glaucoma

Of the several causes for glaucoma, ocular hypertension (increased pressure within the eye) is the
most important risk factor in most glaucomas, but in some populations, only 50% of people with
primary open-angle glaucoma actually have elevated ocular pressure. [12]
Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. Closed-angle
glaucoma accounts for less than 10% of glaucoma cases in the United States, but as many as half
of glaucoma cases in other nations (particularly East Asian countries).
Dietary[edit]
No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that
oral vitamin supplementation is not a recommended treatment for glaucoma.
[13]
 Caffeine increases intraocular pressure in those with glaucoma, but does not appear to affect
normal individuals.[14]
Ethnicity[edit]
Many people of East Asian descent are prone to developing angle closure glaucoma due to
shallower anterior chamber depths, with the majority of cases of glaucoma in this population
consisting of some form of angle closure.[15] Higher rates of glaucoma have also been reported
for Inuit populations, compared to white populations, in Canada and Greenland. [16]
Genetics[edit]
Positive family history is a risk factor for glaucoma. The relative risk of having primary open-angle
glaucoma (P.O.A.G.) is increased about two- to four-fold for people who have a sibling with
glaucoma.[17] Glaucoma, particularly primary open-angle glaucoma, is associated with mutationsin
several genes, including MYOC, ASB10, WDR36, NTF4, TBK1,[18] and RPGRIP1,[19] although most
cases of glaucoma do not involve these genetic mutations. Normal-tension glaucoma, which
comprises one-third of POAG, is also associated with genetic mutations
(including OPA1and OPTN genes).[20]
Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally,
failure of the normal third-trimester gestational atrophy of the hyaloid canal and the tunica vasculosa
lentis is associated with other anomalies. Angle closure-induced ocular hypertension and
glaucomatous optic neuropathy may also occur with these anomalies, [21][22][23] and has been modelled
in mice.[24]
Other[edit]
Other factors can cause glaucoma, known as "secondary glaucoma", including prolonged use
of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such
as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular
trauma (angle-recession glaucoma); and inflammation of the middle layer of the pigmented vascular
eye structure (uveitis), known as uveitic glaucoma.

Pathophysiology[edit]

Human eye cross-sectional view

The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact
etiology. However, the major risk factor for most glaucomas and the focus of treatment is increased
intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by
the ciliary processes of the eye, and its drainage through the trabecular meshwork. Aqueous humor
flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and
the zonules of Zinn, and anteriorly by the iris. It then flows through the pupil of the iris into
the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here, the
trabecular meshwork drains aqueous humor via the scleral venous sinus (Schlemm's canal)
into scleral plexuses and general blood circulation. [25]
In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the
degeneration and obstruction of the trabecular meshwork, whose original function is to absorb the
aqueous humor. Loss of aqueous humor absorption leads to increased resistance and thus a
chronic, painless buildup of pressure in the eye. [26]
In close/narrow-angle, the iridocorneal angle is completely closed because of forward displacement
of the final roll and root of the iris against the cornea, resulting in the inability of the aqueous fluid to
flow from the posterior to the anterior chamber and then out of the trabecular network. This
accumulation of aqueous humor causes an acute increase in pressure and pain.
The inconsistent relationship of glaucomatous optic neuropathy with increased intraocular pressure
has provoked hypotheses and studies on anatomic structure, eye development, nerve compression
trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon
degeneration, glial support cell, immune system, aging mechanisms of neuron loss, and severing of
the nerve fibers at the scleral edge. [27][28][29][30][31][32][33][34][35][36][37]

Diagnosis[edit]
Screening for glaucoma is usually performed as part of a standard eye examination performed
by optometrists and ophthalmologists. Testing for glaucoma should include measurements of the
intraocular pressure via tonometry,[38] anterior chamber angle examination or gonioscopy, and
examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc
ratio and also rim appearance and vascular change. A formal visual field test should be performed.
The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence
tomography, scanning laser polarimetry, and/or scanning laser ophthalmoscopy (Heidelberg retinal
tomogram).[39][40][41]
Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as
Goldmann tonometry should be augmented with pachymetry to measure the central corneal
thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than the
'true' pressure whereas a thinner-than-average cornea can produce a pressure reading lower than
the 'true' pressure.
Because pressure measurement error can be caused by more than just CCT (i.e., corneal hydration,
elastic properties, etc.), it is impossible to 'adjust' pressure measurements based only on CCT
measurements. The frequency doubling illusion can also be used to detect glaucoma with the use of
a frequency doubling technology perimeter. [42]
Examination for glaucoma also could be assessed with more attention given to sex, race, history of
drug use, refraction, inheritance and family history. [39]

Glaucoma tests[43][44]

What test
How it is accomplished
examines

The eye is numbed via eye drops. The examiner then


uses a tonometer to measure the inner pressure of the
Tonometry Inner eye pressure
eye through pressure applied by a puff of warm air or a
tiny tool.

The pupil is dilated via the application of eye drops.


Ophthalmoscopy (dilated eye Shape and color of Using a small magnification device with a light on the
examination) the optic nerve end, the examiner can examine the magnified optic
nerve.

The patient looks straight ahead and is asked to indicate


Complete field of when light passes the patient's peripheral field of vision.
Perimetry (visual field test)
vision This allows the examiner to map the patient’s field of
vision.

Gonioscopy Angle in the eye Eyedrops are used to numb the eye. A hand-held contact
where the iris meets lens with a mirror is placed gently on the eye to allow
the cornea the examiner to see the angle between the cornea and
the iris.

Thickness of the The examiner places a pachymeter gently on the front of


Pachymetry
cornea the eye to measure its thickness.

Thickness of the Using one of several techniques, the nerve fibers are
Nerve fiber analysis
nerve fiber layer examined.

Glaucoma has been classified into specific types:[45]


Primary glaucoma and its variants[edit]
Primary glaucoma (H40.1-H40.2)

 Primary open-angle glaucoma, also known as chronic open-angle


glaucoma, chronic simple glaucoma, glaucoma simplex

 High-tension glaucoma
 Low-tension glaucoma

 Primary angle closure glaucoma, also known as primary closed-


angle glaucoma, narrow-angle glaucoma, pupil-block glaucoma,
acute congestive glaucoma

 Acute angle closure glaucoma (aka AACG)[46]


 Chronic angle closure glaucoma
 Intermittent angle closure glaucoma
 Superimposed on chronic open-angle closure glaucoma
("combined mechanism" – uncommon)
Variants of primary glaucoma

 Pigmentary glaucoma
 Exfoliation glaucoma, also known as pseudoexfoliative
glaucoma or glaucoma capsulare
 Primary juvenile glaucoma
Primary angle closure glaucoma is caused by contact
between the iris and trabecular meshwork, which in turn
obstructs outflow of the aqueous humor from the eye. This
contact between iris and trabecular meshwork (TM) may
gradually damage the function of the meshwork until it fails to
keep pace with aqueous production, and the pressure rises. In
over half of all cases, prolonged contact between iris and TM
causes the formation of synechiae (effectively "scars").
These cause permanent obstruction of aqueous outflow. In
some cases, pressure may rapidly build up in the eye, causing
pain and redness (symptomatic, or so-called "acute" angle
closure). In this situation, the vision may become blurred, and
halos may be seen around bright lights. Accompanying
symptoms may include a headache and vomiting.
Diagnosis is made from physical signs and symptoms: pupils
mid-dilated and unresponsive to light, cornea edematous
(cloudy), reduced vision, redness, and pain. However, the
majority of cases are asymptomatic. Prior to the very severe
loss of vision, these cases can only be identified by
examination, generally by an eye care professional.
Once any symptoms have been controlled, the first line (and
often definitive) treatment is laser iridotomy. This may be
performed using either Nd:YAG or argon lasers, or in some
cases by conventional incisional surgery. The goal of treatment
is to reverse and prevent, contact between the iris and
trabecular meshwork. In early to moderately advanced cases,
iridotomy is successful in opening the angle in around 75% of
cases. In the other 25%, laser iridoplasty, medication
(pilocarpine) or incisional surgery may be required.
Primary open-angle glaucoma is when optic nerve damage
results in a progressive loss of the visual field. [47] This is
associated with increased pressure in the eye. Not all people
with primary open-angle glaucoma have eye pressure that is
elevated beyond normal, but decreasing the eye pressure
further has been shown to stop progression even in these
cases.
The increased pressure is caused by trabecular meshwork
blockage. Because the microscopic passageways are blocked,
the pressure builds up in the eye and causes imperceptible very
gradual vision loss. Peripheral vision is affected first, but
eventually the entire vision will be lost if not treated.
Diagnosis is made by looking for cupping of the optic nerve.
Prostaglandin agonists work by opening uveoscleral
passageways. Beta-blockers, such as timolol, work by
decreasing aqueous formation. Carbonic anhydrase inhibitors
decrease bicarbonate formation from ciliary processes in the
eye, thus decreasing the formation of Aqueous humor.
Parasympathetic analogs are drugs that work on the trabecular
outflow by opening up the passageway and constricting the
pupil. Alpha 2 agonists (brimonidine, apraclonidine) both
decrease fluid production (via. inhibition of AC) and increase
drainage.
Developmental glaucoma[edit]
Developmental glaucoma (Q15.0)

 Primary congenital glaucoma


 Infantile glaucoma
 Glaucoma associated with hereditary or familial diseases
Secondary glaucoma[edit]
Secondary glaucoma (H40.3-H40.6)

 Inflammatory glaucoma

 Uveitis of all types


 Fuchs heterochromic iridocyclitis

 Phacogenic glaucoma

 Angle-closure glaucoma with mature cataract


 Phacoanaphylactic glaucoma secondary to rupture of lens
capsule
 Phacolytic glaucoma due to phacotoxic meshwork blockage
 Subluxation of lens

 Glaucoma secondary to intraocular hemorrhage

 Hyphema
 Hemolytic glaucoma, also known as erythroclastic glaucoma

 Traumatic glaucoma

 Angle recession glaucoma: Traumatic recession on anterior


chamber angle
 Postsurgical glaucoma

 Aphakic pupillary block


 Ciliary block glaucoma

 Neovascular glaucoma (see below for


more details)
 Drug-induced glaucoma

 Corticosteroid induced glaucoma


 Alpha-chymotrypsin glaucoma. Postoperative ocular
hypertension from use of alpha chymotrypsin.

 Glaucoma of miscellaneous origin

 Associated with intraocular tumors


 Associated with retinal detachments
 Secondary to severe chemical burns of the eye
 Associated with essential iris atrophy
 Toxic glaucoma
Neovascular glaucoma, an
uncommon type of glaucoma, is
difficult or nearly impossible to treat,
and is often caused by
proliferative diabetic retinopathy (PDR)
or central retinal vein
occlusion (CRVO). It may also be
triggered by other conditions that result
in ischemia of the retina or ciliary body.
Individuals with poor blood flow to the
eye are highly at risk for this condition.
Neovascular glaucoma results when
new, abnormal vessels begin
developing in the angle of the eye that
begin blocking the drainage. Patients
with such condition begin to rapidly
lose their eyesight. Sometimes, the
disease appears very rapidly,
especially after cataract surgery
procedures. A new treatment for this
disease, as first reported by Kahook
and colleagues, involves the use of a
novel group of medications known
as anti-VEGF agents. These injectable
medications can lead to a dramatic
decrease in new vessel formation and,
if injected early enough in the disease
process, may lead to normalization of
intraocular pressure. Currently, there
are no high-quality controlled trials
demonstrating a beneficial effect of
anti-VEGF treatments in lowering IOP
in people with neovascular glaucoma.
[48]

Toxic glaucoma is open angle


glaucoma with an unexplained
significant rise of intraocular pressure
following unknown pathogenesis.
Intraocular pressure can sometimes
reach 80 mmHg (11 kPa). It
characteristically manifests as ciliary
body inflammation and massive
trabecular oedema that sometimes
extends to Schlemm's canal. This
condition is differentiated from
malignant glaucoma by the presence
of a deep and clear anterior chamber
and a lack of aqueous misdirection.
Also, the corneal appearance is not as
hazy. A reduction in visual acuity can
occur followed neuroretinal
breakdown.
Associated factors include
inflammation, drugs, trauma and
intraocular surgery, including cataract
surgery and vitrectomy procedures.
Gede Pardianto (2005) reported on
four patients who had toxic glaucoma.
One of them underwent
phacoemulsification with small particle
nucleus drops. Some cases can be
resolved with some medication,
vitrectomy procedures or
trabeculectomy. Valving procedures
can give some relief, but further
research is required.[49]
Absolute glaucoma[edit]
Absolute glaucoma (H44.5) is the end
stage of all types of glaucoma. The
eye has no vision, absence of pupillary
light reflex and pupillary response, and
has a stony appearance. Severe pain
is present in the eye. The treatment of
absolute glaucoma is a destructive
procedure like cyclocryoapplication,
cyclophotocoagulation, or injection of
99% alcohol.
Types[edit]
This section needs additional citations
for verification. Please help improve this
article by adding citations to reliable
sources. Unsourced material may be
challenged and removed. (August
2015) (Learn how and when to remove this
template message)

Glaucoma is an umbrella term for eye


conditions which damage the optic
nerve, and which can lead to a loss of
vision.[50] The main cause of damage to
the optic nerve is intraocular pressure
(IOP), excessive fluid pressure within
the eye, which can be due to various
reasons including blockage of drainage
ducts, and narrowing or closure of the
angle between the iris and cornea.
The primary division in categorizing
different types of glaucoma is open-
angle and closed-angle (or angle-
closure) glaucoma. The open angle
refers to the angle where the iris meets
the cornea being as wide and open as
it should be, allowing the fluid from
inside the eye to drain, thus relieving
the internal pressure. Where this angle
is narrowed or closed, pressure can
build up, and eventually damage the
optic nerve leading to loss of vision.
Primary open-angle glaucoma
(also, primary glaucoma, chronic
glaucoma) refers to slow clogging of
the drainage canals resulting in
increased eye pressure which causes
progressive optic nerve damage. This
manifests as a gradual loss of the
visual field, starting with a loss
of peripheral vision, but eventually the
entire vision will be lost if not treated.
[47]
 This is the most common type of
glaucoma, accounting for 90% of
cases in the United States, but fewer in
Asian countries. Onset is slow and
painless, and loss of vision is gradual
and irreversible.
Narrow-angle glaucoma (also closed-
angle glaucoma) the iris bows forward,
narrowing the angle that drains the
eye, increasing pressure within the
eye. If untreated, it can lead to the
medical emergency of angle-closure
glaucoma.
In angle-closure glaucoma
(also closed-angle glaucoma, primary
angle-closure glaucoma, acute
glaucoma) the iris bows forward and
causes physical contact between the
iris and trabecular meshwork, which
blocks the outflow of aqueous humor
from within the eye. This contact may
gradually damage the draining function
of the meshwork until it fails to keep
pace with aqueous production, and the
intraocular pressure rises. The onset of
symptoms is sudden and causes pain
and other symptoms that are
noticeable; it is treated as a medical
emergency. Unlike open-angle
glaucoma, angle-closure glaucoma is a
result of the angle between the iris and
cornea closing. This tends to occur in
the far-sighted, who have smaller-than-
normal anterior chambers, making
physical contact between the iris and
trabecular meshwork more likely.
Normal-tension glaucoma
(also NTG, low-tension
glaucoma, normal-pressure glaucoma)
is a condition where the optic nerve is
damaged although intraocular
pressure (IOP) is in the normal range
(12-22mm Hg). Individuals with a
family history of NTG, those of
Japanese ancestry, and those with a
history of systemic heart disease are at
higher than average risk of developing
NTG. The cause of NTG is unknown.
Secondary glaucoma refers to any
case in which another disease, trauma,
drug or procedure causes increased
eye pressure, resulting in optic nerve
damage and vision loss, and may be
mild or severe. It can be due to an eye
injury, inflammation, a tumor, or
advanced cases of cataracts or
diabetes. It can also be caused by
certain drugs such as steroids.
Treatment depends on whether it is
open-angle or angle-closure glaucoma.
In pseudoexfoliation
glaucoma (also, PEX, exfoliation
glaucoma) the pressure is due to the
accumulation of microscopic granular
protein fibers, which can block normal
drainage of the aqueous humor. PEX
is prevalent in Scandinavia, primarily in
those over 70, and more commonly in
women.
Pigmentary glaucoma (also,
pigmentary dispersion syndrome) is
caused by pigment cells sloughing off
from the back of the iris and floating
around in the aqueous humor. Over
time, these pigment cells can
accumulate in the anterior chamber in
such a way that it can begin to clog the
trabecular meshwork. It is a rare
condition that occurs mostly among
Caucasians, mostly males in their mid-
20s to 40s, and most are nearsighted.
Primary juvenile glaucoma is a
neonate or juvenile abnormality where
ocular hypertension is evident at birth
or shortly thereafter and is caused by
abnormalities in the anterior chamber
angle development that blocks the
outflow of the aqueous humor.
Uveitic Glaucoma is due to uveitis, the
swelling and inflammation of the uvea,
the middle layer of the eye. The uvea
provides most of the blood supply to
the retina. Increased eye pressure in
uveitis can result from the inflammation
itself or from the steroids used to treat
it.

Screening[edit]
The United States Preventive Services
Task Force as of 2013 states there is
insufficient evidence to recommend for
or against screening for glaucoma.
[51]
 Therefore, there is no national
screening program in the US.
Screening, however, is recommended
starting at age 40 by the American
Academy of Ophthalmology.[2]
There is a glaucoma screening
program in the UK. Those at risk are
advised to have a dilated eye
examination at least once a year.[52]

Treatment[edit]
The modern goals of glaucoma
management are to avoid
glaucomatous damage and nerve
damage, and preserve visual field and
total quality of life for patients, with
minimal side effects.[53][54] This requires
appropriate diagnostic techniques and
follow-up examinations, and judicious
selection of treatments for the
individual patient. Although intraocular
pressure is only one of the major risk
factors for glaucoma, lowering it via
various pharmaceuticals and/or
surgical techniques is currently the
mainstay of glaucoma treatment.
Vascular flow and neurodegenerative
theories of glaucomatous optic
neuropathy have prompted studies on
various neuroprotective therapeutic
strategies, including nutritional
compounds, some of which may be
regarded by clinicians as safe for use
now, while others are on trial.
Medication[edit]
Latanoprost

Main article: Glaucoma medication


Intraocular pressure can be lowered
with medication, usually eye drops.
Several classes of medications are
used to treat glaucoma, with several
medications in each class.
Each of these medicines may have
local and systemic side effects.
Adherence to medication protocol can
be confusing and expensive; if side
effects occur, the patient must be
willing either to tolerate them or to
communicate with the treating
physician to improve the drug regimen.
Initially, glaucoma drops may
reasonably be started in either one or
in both eyes.[55] Wiping the eye with an
absorbent pad after the administration
of eye drops may result in fewer
adverse effects, like the growth of
eyelashes and hyperpigmentation in
the eyelid.[56]
Poor compliance with medications and
follow-up visits is a major reason for
vision loss in glaucoma patients. A
2003 study of patients in
an HMO found half failed to fill their
prescriptions the first time, and one-
fourth failed to refill their prescriptions
a second time.[57] Patient education and
communication must be ongoing to
sustain successful treatment plans for
this lifelong disease with no early
symptoms.
The possible neuroprotective effects of
various topical and systemic
medications are also being
investigated.[13][58][59][60]
 Prostaglandin analogs, such
as latanoprost, bimatoprost and tra
voprost, increase uveoscleral
outflow of aqueous humor.
Bimatoprost also increases
trabecular outflow.
 Topical beta-adrenergic receptor
antagonists, such
as timolol, levobunolol,
and betaxolol, decrease aqueous
humor production by the
epithelium of the ciliary body.
 Alpha2-adrenergic agonists, such
as brimonidine and apraclonidine,
work by a dual mechanism,
decreasing aqueous humor
production and increasing
uveoscleral outflow.
 Less-selective alpha agonists,
such as epinephrine, decrease
aqueous humor production
through vasoconstriction of ciliary
body blood vessels, useful only in
open-angle glaucoma.
Epinephrine's mydriatic effect,
however, renders it unsuitable for
closed-angle glaucoma due to
further narrowing of the
uveoscleral outflow (i.e. further
closure of trabecular meshwork,
which is responsible for absorption
of aqueous humor).
 Miotic
agents (parasympathomimetics),
such as pilocarpine, work by
contraction of the ciliary muscle,
opening the trabecular
meshwork and allowing increased
outflow of the aqueous
humour. Echothiophate, an
acetylcholinesterase inhibitor, is
used in chronic glaucoma.
 Carbonic anhydrase inhibitors,
such
as dorzolamide, brinzolamide,
and acetazolamide, lower
secretion of aqueous humor by
inhibiting carbonic anhydrase in
the ciliary body.
Laser[edit]
Argon laser trabeculoplasty (ALT) may
be used to treat open-angle glaucoma,
but this is a temporary solution, not a
cure. A 50-μm argon laser spot is
aimed at the trabecular meshwork to
stimulate the opening of the mesh to
allow more outflow of aqueous fluid.
Usually, half of the angle is treated at a
time. Traditional laser trabeculoplasty
uses a thermal argon laser in
an argon laser trabeculoplasty
procedure.
A newer type of laser trabeculoplasty
uses a "cold" (nonthermal) laser to
stimulate drainage in the trabecular
meshwork. This newer procedure,
selective laser trabeculoplasty (SLT),
uses a 532-nm, frequency-doubled, Q-
switched Nd:YAG laser, which
selectively targets melanin pigment in
the trabecular meshwork cells. Studies
show SLT is as effective as ALT at
lowering eye pressure. In addition, SLT
may be repeated three to four times,
whereas ALT can usually be repeated
only once.
Nd:YAG laser peripheral iridotomy
(LPI) may be used in patients
susceptible to or affected by angle
closure glaucoma or pigment
dispersion syndrome. During laser
iridotomy, laser energy is used to
make a small, full-thickness opening in
the iris to equalize the pressure
between the front and back of the iris,
thus correcting any abnormal bulging
of the iris. In people with narrow
angles, this can uncover the trabecular
meshwork. In some cases of
intermittent or short-term angle
closure, this may lower the eye
pressure. Laser iridotomy reduces the
risk of developing an attack of acute
angle closure. In most cases, it also
reduces the risk of developing chronic
angle closure or of adhesions of the
iris to the trabecular meshwork.
Diode laser cycloablation lowers IOP
by reducing aqueous secretion by
destroying secretory ciliary epithelium.
[39]
Surgery[edit]

Conventional surgery to treat


glaucoma makes a new opening in
the trabecular meshwork, which helps
fluid to leave the eye and lowers
intraocular pressure.

Main article: Glaucoma surgery


Both laser and conventional surgeries
are performed to treat glaucoma.
Surgery is the primary therapy for
those with congenitalglaucoma.
[61]
 Generally, these operations are a
temporary solution, as there is not yet
a cure for glaucoma.
Canaloplasty[edit]
Canaloplasty is a nonpenetrating
procedure using
microcatheter technology. To perform
a canaloplasty, an incision is made into
the eye to gain access to the
Schlemm's canal in a similar fashion to
a viscocanalostomy. A microcatheter
will circumnavigate the canal around
the iris, enlarging the main drainage
channel and its smaller collector
channels through the injection of a
sterile, gel-like material called
viscoelastic. The catheter is then
removed and a suture is placed within
the canal and tightened.
By opening the canal, the pressure
inside the eye may be relieved,
although the reason is unclear, since
the canal (of Schlemm) does not have
any significant fluid resistance in
glaucoma or healthy eyes. Long-term
results are not available.[62][63]
Trabeculectomy[edit]
The most common conventional
surgery performed for glaucoma is
the trabeculectomy. Here, a partial
thickness flap is made in the scleral
wall of the eye, and a window opening
is made under the flap to remove a
portion of the trabecular meshwork.
The scleral flap is then sutured loosely
back in place to allow fluid to flow out
of the eye through this opening,
resulting in lowered intraocular
pressure and the formation of a bleb or
fluid bubble on the surface of the eye.
Scarring can occur around or over the
flap opening, causing it to become less
effective or lose effectiveness
altogether. Traditionally,
chemotherapeutic adjuvants, such
as mitomycin C (MMC) or 5-
fluorouracil (5-FU), are applied with
soaked sponges on the wound bed to
prevent filtering blebs from scarring by
inhibiting fibroblast proliferation.
Contemporary alternatives to prevent
the scarring of the meshwork opening
include the sole or combinative
implementation of
nonchemotherapeutic adjuvants such
as the ologen collagen matrix, which
has been clinically shown to increase
the success rates of surgical
treatment.[64][65][66][67]
Collagen matrix prevents scarring by
randomizing and modulating fibroblast
proliferation in addition to mechanically
preventing wound contraction and
adhesion.
Glaucoma drainage implants[edit]
Main article: Glaucoma valve
Professor Anthony Molteno developed
the first glaucoma drainage implant,
in Cape Town in 1966.[68] Since then,
several types of implants have
followed on from the original, the
Baerveldt tube shunt, or the valved
implants, such as the Ahmed
glaucoma valve implant or the ExPress
Mini Shunt and the later generation
pressure ridge Molteno implants.
These are indicated for glaucoma
patients not responding to maximal
medical therapy, with previous failed
guarded filtering surgery
(trabeculectomy). The flow tube is
inserted into the anterior chamber of
the eye, and the plate is implanted
underneath the conjunctiva to allow a
flow of aqueous fluid out of the eye into
a chamber called a bleb.

 The first-generation Molteno and


other nonvalved implants
sometimes require the ligation of
the tube until the bleb formed is
mildly fibrosed and water-tight.
[69]
 This is done to reduce
postoperative hypotony—sudden
drops in postoperative intraocular
pressure.
 Valved implants, such as the
Ahmed glaucoma valve, attempt to
control postoperative hypotony by
using a mechanical valve.
 Ab interno implants, such as the
Xen Gel Stent, are transscleral
implants by an ab interno
procedure to channel aqueous
humor into the non-dissected
Tenon's space, creating a
subconjunctival drainage area
similar to a bleb.[70][71] The implants
are transscleral and different from
more other ab interno implants that
do not create a transscleral
drainage, such as iStent, CyPass,
or Hydrus.[72]
The ongoing scarring over the
conjunctival dissipation segment of the
shunt may become too thick for the
aqueous humor to filter through. This
may require preventive measures
using antifibrotic medications, such
as 5-fluorouracil or mitomycin-C (durin
g the procedure), or other
nonantifibrotic medication methods,
such as collagen matrix implant, [73][74] or
biodegradable spacer, or later on
create a necessity for revision surgery
with the sole or combinative use of
donor patch grafts or collagen matrix
implant.[75][76] And for glaucomatous
painful blind eye and some cases of
glaucoma, cyclocryotherapy for ciliary
body ablation could be considered to
be performed.[77]
Laser-assisted nonpenetrating deep
sclerectomy[edit]
The most common surgical approach
currently used for the treatment of
glaucoma is trabeculectomy, in which
the sclera is punctured to alleviate
intraocular pressure.
Nonpenetrating deep sclerectomy
(NPDS) surgery is a similar, but
modified, procedure, in which instead
of puncturing the scleral bed and
trabecular meshwork under a scleral
flap, a second deep scleral flap is
created, excised, with further
procedures of deroofing the Schlemm's
canal, upon which, percolation of liquid
from the inner eye is achieved and
thus alleviating intraocular pressure,
without penetrating the eye. NPDS is
demonstrated to have significantly
fewer side effects than trabeculectomy.
[78]
 However, NPDS is performed
manually and requires higher level of
skills that may be assisted with
instruments.[citation needed] In order to prevent
wound adhesion after deep scleral
excision and to maintain good filtering
results, NPDS as with other non-
penetrating procedures is sometimes
performed with a variety of
biocompatible spacer or devices, such
as the Aquaflow collagen wick,
[79]
ologen Collagen Matrix,[66][80][81] or
Xenoplast glaucoma implant.[82]
Laser-assisted NPDS is performed
with the use of a CO2 laser system.
The laser-based system is self-
terminating once the required scleral
thickness and adequate drainage of
the intraocular fluid have been
achieved. This self-regulation effect is
achieved as the CO2 laser essentially
stops ablating as soon as it comes in
contact with the intraocular percolated
liquid, which occurs as soon as the
laser reaches the optimal residual
intact layer thickness.

Prognosis[edit]
In open-angle glaucoma, the typical
progression from normal vision to
complete blindness takes about 25
years to 70 years without treatment,
depending on the method of estimation
used.[83] The intraocular pressure can
also have an effect, with higher
pressures reducing the time until
blindness.[84]

Epidemiology[edit]

Disability-adjusted life year for


glaucoma per 100,000 inhabitants in
2004[85]
  no data
  fewer than 20
  20–43
  43–66
  66–89
  89–112
  112–135
  135–158
  158–181
  181–204
  204–227
  227–250
  more than 250

As of 2010, there were 44.7 million


people in the world with open angle
glaucoma.[86] The same year, there
were 2.8 million people in the United
States with open angle glaucoma. [86] By
2020, the prevalence is projected to
increase to 58.6 million worldwide and
3.4 million the United States.[86]
Both internationally and in the United
States glaucoma is the second-leading
cause of blindness.
[2]
 Globally cataracts are a more
common cause. Glaucoma is also the
leading cause of blindness in African
Americans, who have higher rates of
primary open angle glaucoma.[87]
[88]
 Bilateral vision loss can negatively
affect mobility and interfere with
driving.[89]
A meta-analysis published in 2009
found that people with primary open
angle glaucoma do not have
increased mortality rates, or increased
risk of cardiovascular death. [90]

History[edit]
The association of elevated intraocular
pressure (IOP) and the eye disease
glaucoma was first described by
Englishman Richard Bannister in 1622:
"...that the Eye be grown more solid
and hard, then naturally it should be...".
[91]
 Angle-closure glaucoma was treated
with cataract extraction by John Collins
Warren in Boston as early as 1806.
[92]
 The invention of the
ophthalmoscope by Hermann
Helmholtz in 1851 enabled
ophthalmologists for the first time to
identify the pathological hallmark of
glaucoma, the excavation of the optic
nerve head due to retinal ganglion cell
loss. The first reliable instrument to
measure intraocular pressure was
invented by Norwegian
ophthalmologist Hjalmar August
Schiøtz in 1905. About half a century
later, Hans Goldmann in Berne,
Switzerland, developed his applanation
tonometer which still today - despite
numerous new innovations in
diagnostics - is considered the gold
standard of determining this crucial
pathogenic factor. In the late 20th
century, further pathomechanisms
beyond elevated IOP were discovered
and became the subject of research
like insufficient blood supply – often
associated with low or irregular blood
pressure – to the retina and optic
nerve head.[93] The first drug to reduce
IOP, pilocarpine, was introduced in the
1870s. Early surgical techniques like
iridectomy and fistulating methods
have recently been supplemented by
less invasive procedures like small
implants, a range of options now
widely called MIGS (micro-invasive
glaucoma surgery).
Etymology[edit]
The word "glaucoma" comes from
the Greek γλαύκωμα,[94][95] a derivative
of γλαυκóς,[96] which commonly
described the color of eyes which were
not dark (i.e. blue, green, light gray).
Eyes described as γλαυκóς due to
disease might have had a gray
cataract in the Hippocratic era, or, in
the early Common Era, the greenish
pupillary hue sometimes seen in angle-
closure glaucoma.[9][97]

Research[edit]
Scientists track eye movements in
glaucoma patients to check vision
impairment while driving

Rho kinase inhibitors[edit]


Rho kinase inhibitors, such
as ripasudil, work by inhibition of the
actin cytoskeleton, resulting in the
morphological changes in the
trabecular meshwork and increased
aqueous outflow. More compounds in
this class are being investigated in
phase 2 and phase 3 trials.[98]
Neuroprotective agents[edit]
A 2013 Cochrane Systematic
Review compared the effect of
brimonidine and timolol in slowing the
progression of open angle glaucoma in
adult participants.[99] The results
showed that participants assigned to
brimonidine showed less visual field
progression that those assigned to
timolol, though the results were not
significant, given the heavy loss-to-
followup and limited evidence.[99] The
mean intraocular pressures for both
groups were similar. Participants in the
brimonidine group had a higher
occurrence of side effects caused by
medication than participants in the
timolol group.[99]
Cannabis[edit]
Studies in the 1970s reported that the
use of cannabis may lower intraocular
pressure.[100][101][102] In an effort to
determine whether marijuana, or drugs
derived from it, might be effective as a
glaucoma treatment, the US National
Eye Institute supported research
studies from 1978 to 1984. These
studies demonstrated some derivatives
of marijuana lowered intraocular
pressure when administered orally,
intravenously, or by smoking, but not
when topically applied to the eye.
In 2003, the American Academy of
Ophthalmology released a position
statement stating that cannabis was
not more effective than prescription
medications. Furthermore, no scientific
evidence has been found that
demonstrates increased benefits
and/or diminished risks of cannabis
use to treat glaucoma compared with
the wide variety of pharmaceutical
agents now available.[102][103]
In 2012 the American Glaucoma
Society published a position paper
discrediting the use of cannabis as a
legitimate treatment for elevated
intraocular pressure, for reasons
including short duration of action and
side effects that limit many activities of
daily living.[104]

References[edit]
1. ^ Jump up
to:a b c d e f g h i j k l m n o "Facts About
Glaucoma". National Eye
Institute. Archivedfrom the original
on 28 March 2016. Retrieved 29
March 2016.
2. ^ Jump up
to:a b c d e f g h i j k l m n o p q r s Mantrav
adi, AV; Vadhar, N (September
2015). "Glaucoma". Primary Care.
Saunders (Elsevier). 42 (3): 437–
49. doi:10.1016/j.pop.2015.05.00
8. ISSN 0095-4543. PMID 26319
348 – via Elsevier Science
Direct. (Subscription required (help)).
3. Jump up^ Ferri, Fred F.
(2010). Ferri's differential
diagnosis : a practical guide to the
differential diagnosis of
symptoms, signs, and clinical
disorders (2nd ed.). Philadelphia,
PA: Elsevier/Mosby. p. Chapter
G. ISBN 0323076998.
4. ^ Jump up to:a b GBD 2015
Disease and Injury Incidence and
Prevalence, Collaborators. (8
October 2016). "Global, regional,
and national incidence,
prevalence, and years lived with
disability for 310 diseases and
injuries, 1990–2015: a systematic
analysis for the Global Burden of
Disease Study
2015". Lancet. 388 (10053):
1545–1602. PMID 27733282.
5. Jump up^ Rhee, Douglas J.
(2012). Glaucoma (2 ed.).
Philadelphia: Wolters Kluwer
Health/Lippincott Williams &
Wilkins.
p. 180. ISBN 9781609133375. O
CLC 744299538.
6. Jump up^ Mi, Xue-Song; Yuan,
Ti-Fei; So, Kwok-Fai (16
September 2014). "The current
research status of normal tension
glaucoma". Clinical Interventions
in Aging. 9: 1563–
71. doi:10.2147/CIA.S67263. PM
C 4172068  . PMID 25258525.
7. Jump up^ "Glaucoma: The 'silent
thief' begins to tell its
secrets" (Press release). National
Eye Institute. 21 January
2014. Archived from the original
on 23 July 2015.
8. Jump up^ Resnikoff, Serge;
Pascolini, Donatella; Etya'Ale,
Daniel; Kocur, Ivo;
Pararajasegaram, Ramachandra;
Pokharel, Gopal P.; Mariotti,
Silvio P. (2004). "Global data on
visual impairment in the year
2002". Bulletin of the World
Health Organization. 82 (11):
844–51. doi:10.1590/S0042-
96862004001100009. PMC 2623
053  . PMID 15640920. Archived 
from the original on 2013-12-12.
9. ^ Jump up to:a b Leffler, CT;
Schwartz, SG; Giliberti, FM;
Young, MT; Bermudez, D
(2015). "What was Glaucoma
Called Before the 20th
Century?". Ophthalmology and
Eye Diseases. Libertas
Academica. 7: 21–
33. doi:10.4137/OED.S32004. IS
SN 1179-1721. PMC 4601337 
. PMID 26483611. Archived from
the original on 2016-04-23.
10. Jump up^ Leffler CT, Schwartz
SG, Stackhouse R, Davenport B,
Spetzler K (2013). "Evolution and
impact of eye and vision terms in
written English". JAMA
Ophthalmology. 131 (12): 1625–
31. doi:10.1001/jamaophthalmol.2
013.917. PMID 24337558. Archiv
ed from the original on 2014-12-
23.
11. Jump up^ Friedman, Neil J.;
Kaiser, Peter K.; II, Roberto
Pineda (2014). The
Massachusetts Eye and Ear
Infirmary Illustrated Manual of
Ophthalmology E-Book. Elsevier
Health Sciences.
p. 234. ISBN 9780323225274.
12. Jump up^ Sommer A, Tielsch
JM, Katz J, et al. (August 1991).
"Relationship between intraocular
pressure and primary open angle
glaucoma among white and black
Americans. The Baltimore Eye
Survey". Archives of
Ophthalmology. 109 (8): 1090–
95. doi:10.1001/archopht.1991.01
080080050026. PMID 1867550. (
Subscription required (help)).
13. ^ Jump up to:a b Rhee DJ, Katz LJ,
Spaeth GL, Myers JS (2001).
"Complementary and alternative
medicine for glaucoma". Survey
of Ophthalmology. 46 (1): 43–
55. doi:10.1016/S0039-
6257(01)00233-8. PMID 1152579
0. (Subscription required (help)).
14. Jump up^ Li, M; Wang, M; Guo,
W; Wang, J; Sun, X (March
2011). "The effect of caffeine on
intraocular pressure: a systematic
review and meta-
analysis". Graefe's archive for
clinical and experimental
ophthalmology = Albrecht von
Graefes Archiv für klinische und
experimentelle Ophthalmologie.
Springer. 249 (3): 435–
42. doi:10.1007/s00417-010-
1455-1. ISSN 1435-702X. PMID 2
0706731. (Subscription required
(help)).
15. Jump up^ Wang N, Wu H, Fan Z
(November 2002). "Primary angle
closure glaucoma in Chinese and
Western populations". Chinese
Medical Journal. 115 (11): 1706–
15. PMID 12609093. Archived fro
m the original on 2016-12-21.
16. Jump up^ Friedman D, Vedula
SS (2006). "Lens extraction for
chronic angle-closure
glaucoma". Cochrane Database
Syst Rev. 3:
CD005555. doi:10.1002/1465185
8.CD005555.pub2. PMC 4438535
  . PMID 16856103.
17. Jump up^ Myron Yanoff; Jay S.
Duker
(2009). Ophthalmology (3rd ed.).
Mosby Elsevier.
p. 1096. ISBN 9780323043328.
18. Jump up^ Online Mendelian
Inheritance in
Man (OMIM) GLAUCOMA,
PRIMARY OPEN ANGLE; POAG
-137760
19. Jump up^ Fernández-Martínez,
Lorena; Letteboer, Stef; Mardin,
Christian Y.; Weisschuh, Nicole;
Gramer, Eugen; Weber, Bernhard
Hf; Rautenstrauss, Bernd;
Ferreira, Paulo A.; Kruse,
Friedrich E. (April
2011). "Evidence for RPGRIP1
gene as risk factor for primary
open angle glaucoma". European
journal of human genetics:
EJHG. 19 (4): 445–
451. doi:10.1038/ejhg.2010.217. I
SSN 1476-5438. PMC 3060327 
. PMID 21224891.
20. Jump up^ Online Mendelian
Inheritance in
Man (OMIM) GLAUCOMA,
NORMAL TENSION,
SUSCEPTIBILITY TO -606657
21. Jump up^ Pardianto G, et al.
(2005). "Aqueous Flow and the
Glaucoma". Mimbar Ilmiah
Oftalmologi Indonesia. 2: 12–15.
22. Jump up^ Chaum E, et al. "A 5-
year-old girl who failed her school
vision screening. Case
presentation of Persistent fetal
vasculature (PFV), also called
persistent hyperplastic primary
vitreous (PHPV)". Digital Journal
of Ophthalmology. Archived from
the original on 2009-01-11.
23. Jump up^ Hunt A, Rowe N, Lam
A, Martin F (July
2005). "Outcomes in persistent
hyperplastic primary vitreous". Br
J Ophthalmol. 89 (7): 859–
63. doi:10.1136/bjo.2004.053595. 
PMC 1772745  . PMID 15965167
.
24. Jump up^ Chang B, Smith RS,
Peters M, et al.
(2001). "Haploinsufficient Bmp4
ocular phenotypes include
anterior segment dysgenesis with
elevated intraocular
pressure". BMC Genet. 2:
18. doi:10.1186/1471-2156-2-18. 
PMC 59999  . PMID 11722794.
25. Jump up^ Alguire P (1990). "The
Eye Chapter 118
Tonometry>Basic Science". In
Walker HK, Hall WD, Hurst
JW. Clinical methods: the history,
physical, and laboratory
examinations (3rd ed.). London:
Butterworths. ISBN 0-409-90077-
X.
26. Jump up^ Mozaffarieh M,
Grieshaber MC, Flammer J
(2008). "Oxygen and blood flow:
players in the pathogenesis of
glaucoma". Mol Vis. 14: 224–
33. PMC 2267728  . PMID 18334
938. Archived from the original on
2008-06-09.
27. Jump up^ Osborne NN, Wood
JP, Chidlow G, Bae JH, Melena J,
Nash MS (August
1999). "Ganglion cell death in
glaucoma: what do we really
know?". Br J Ophthalmol. 83 (8):
980–6. doi:10.1136/bjo.83.8.980. 
PMC 1723166  . PMID 10413706
.
28. Jump up^ Levin LA, Peeples P
(February 2008). "History of
neuroprotection and rationale as
a therapy for glaucoma". Am J
Manag Care. 14 (1 Suppl): S11–
4. PMID 18284310. Archived from
the original on 2012-04-07.
29. Jump up^ Varma R, Peeples P,
Walt JG, Bramley TJ (February
2008). "Disease progression and
the need for neuroprotection in
glaucoma management". Am J
Manag Care. 14 (1 Suppl): S15–
9. PMID 18284311. Archived from
the original on 2012-04-07.
30. Jump up^ Hernández M, Urcola
JH, Vecino E (May 2008). "Retinal
ganglion cell neuroprotection in a
rat model of glaucoma following
brimonidine, latanoprost or
combined treatments". Exp Eye
Res. 86 (5): 798–
806. doi:10.1016/j.exer.2008.02.0
08. PMID 18394603.
31. Jump up^ Cantor LB (December
2006). "Brimonidine in the
treatment of glaucoma and ocular
hypertension". Ther Clin Risk
Manag. 2 (4): 337–
46. doi:10.2147/tcrm.2006.2.4.33
7. PMC 1936355  . PMID 183606
46.
32. Jump up^ Schwartz M (June
2007). "Modulating the immune
system: a vaccine for
glaucoma?". Can J
Ophthalmol. 42 (3): 439–
41. doi:10.3129/I07-050. PMID 17
508041.
33. Jump up^ Morrison JC
(2006). "INTEGRINS IN THE
OPTIC NERVE HEAD:
POTENTIAL ROLES IN
GLAUCOMATOUS OPTIC
NEUROPATHY (AN AMERICAN
OPHTHALMOLOGICAL
SOCIETY THESIS)". Trans Am
Ophthalmol Soc. 104: 453–
77. PMC 1809896  . PMID 17471
356.
34. Jump up^ Knox DL, Eagle RC,
Green WR (March 2007). "Optic
nerve hydropic axonal
degeneration and blocked
retrograde axoplasmic transport:
histopathologic features in human
high-pressure secondary
glaucoma". Arch
Ophthalmol. 125 (3): 347–
53. doi:10.1001/archopht.125.3.3
47. PMID 17353405.
35. Jump up^ Tezel G, Luo C, Yang
X (March 2007). "Accelerated
Aging in Glaucoma:
Immunohistochemical
Assessment of Advanced
Glycation End Products in the
Human Retina and Optic Nerve
Head". Invest. Ophthalmol. Vis.
Sci. 48 (3): 1201–
11. doi:10.1167/iovs.06-0737. PM
C 2492883  . PMID 17325164.
36. Jump up^ Berry FB, Mirzayans
F, Walter MA (April 2006).
"Regulation of FOXC1 stability
and transcriptional activity by an
epidermal growth factor-activated
mitogen-activated protein kinase
signaling cascade". J Biol
Chem. 281 (15): 10098–
104. doi:10.1074/jbc.M513629200
. PMID 16492674.
37. Jump up^ "Issue on
neuroprotection". Can J
Ophthalmol. 42 (3). June
2007. ISSN 1715-3360. Archived
from the original on 2007-05-12.
38. Jump up^ Farandos, NM;
Yetisen, AK; Monteiro, MJ; Lowe,
CR; Yun, SH (November
2014). "Contact Lens Sensors in
Ocular Diagnostics". Advanced
Healthcare Materials. 4: 792–
810. doi:10.1002/adhm.20140050
4. PMID 25400274. Archived from
the original on 2015-01-02.
39. ^ Jump up to:a b c Pardianto G et
al. Some difficulties on Glaucoma.
Mimbar Ilmiah Oftalmologi
Indonesia.2006;3: 49–52.
40. Jump up^ Thomas R, Parikh RS
(September 2006). "How to
assess a patient for
glaucoma". Community Eye
Health. 19 (59): 36–
7. PMC 1705629  . PMID 174917
13.
41. Jump up^ Michelessi M,
Lucenteforte E, Oddone F,
Brazzelli M, Parravano M, Franchi
S, Ng SM, Virgili G (2015). "Optic
nerve head and fibre layer
imaging for diagnosing
glaucoma". Cochrane Database
Syst Rev. 11:
CD008803. doi:10.1002/1465185
8.CD008803.pub2. PMID 266183
32.
42. Jump up^ Johnson, Chris A. The
use of a visual illusion to detect
glaucoma. In Visual Perception:
The Influence of H. W. Leibowitz,
eds. Andre, J., Owens, D. A., and
Harvey, Jr., L. O. (2003); 45–56.
Washington, D.C.: The American
Psychological Association.
43. Jump up^ Foundation, G. R.
(n.d.). "Five common Glaucoma
Tests".
Glaucoma.org. Archivedfrom the
original on 2017-09-08.
Retrieved 2014-02-20.
44. Jump up^ "Nerve Fiber
Analysis". Glaucoma Associates
of Texas. White Rabbit
Communications, Inc. 2010.
Archived from the original on 26
March 2013. Retrieved 9
December 2012.
45. Jump up^ Paton D, Craig JA;
Craig (1976). "Glaucomas.
Diagnosis and management". Clin
Symp. 28 (2): 1–
47. PMID 1053095.
46. Jump up^ Logan, Carolynn M.;
Rice, M. Katherine
(1987). Logan's Medical and
Scientific Abbreviations.
Philadelphia: J. B. Lippincott
Company. p. 3. ISBN 0-397-
54589-4.
47. ^ Jump up to:a b "Primary Open-
Angle Glaucoma: Glaucoma:
Merck Manual Professional".
Merck.com. Archived from the
original on 2010-11-28.
Retrieved 2011-01-24.
48. Jump up^ Simha A, Braganza A,
Abraham L, Samuel P, Lindsley K
(2013). "Anti-vascular endothelial
growth factor for neovascular
glaucoma". Cochrane Database
Syst Rev. 10:
CD007920. doi:10.1002/1465185
8.CD007920.pub2. PMC 4261636
  . PMID 24089293.
49. Jump up^ Pardianto G,
Difficulties on glaucoma in
Mimbar Ilmiah Oftalmologi
Indonesia.2006;3: 48–9.[verification needed]
50. Jump up^ Arthur J. Sit, MD (April
23, 2006). "Many types of
glaucoma, one kind of damage to
optic nerve". Chicago Tribune.
Archived from the original on
2012-10-06. Retrieved 2015-08-
18. Glaucoma is a broad term for
a number of different conditions
that damage the optic nerve, the
'cable' that carries visual
information from the eye to the
brain, thereby causing changes in
vision.
51. Jump up^ Moyer, Virginia A. (9
July 2013). "Screening for
Glaucoma: U.S. Preventive
Services Task Force
Recommendation
Statement". Annals of Internal
Medicine. doi:10.7326/0003-
4819-159-6-201309170-00685.
52. Jump up^ "Glaucoma – National
Institutes of Health".
Nihseniorhealth.gov. Archived fro
m the original on 2010-12-25.
Retrieved 2011-01-24.
53. Jump up^ Noecker RJ (June
2006). "The management of
glaucoma and intraocular
hypertension: current approaches
and recent advances". Ther Clin
Risk Manag. 2 (2): 193–
206. doi:10.2147/tcrm.2006.2.2.1
93. PMC 1661659  . PMID 18360
593.
54. Jump up^ Parikh RS, Parikh SR,
Navin S, Arun E, Thomas R (1
May 2008). "Practical approach to
medical management of
glaucoma". Indian J
Ophthalmol. 56 (3): 223–
30. doi:10.4103/0301-
4738.40362. PMC 2636120  . P
MID 18417824. Archived from the
original on 19 July 2011.
55. Jump up^ Leffler CT, Amini L
(2007). "Interpretation of uniocular
and binocular trials of glaucoma
medications: an observational
case series". BMC Ophthalmol. 7:
17. doi:10.1186/1471-2415-7-17. 
PMC 2093925  . PMID 17916260
.
56. Jump up^ Xu L, Wang X, Wu M
(2017). "Topical medication
instillation techniques for
glaucoma". Cochrane Database
Syst Rev (2):
CD010520. doi:10.1002/1465185
8.CD010520.pub2. PMID 282184
04.
57. Jump up^ Jaret, Peter. "A New
Understanding of Glaucoma".
NYTimes.com. Archived from the
original on 2014-03-10.
Retrieved 2014-02-20.
58. Jump up^ Ritch R (June 2007).
"Natural compounds: evidence for
a protective role in eye
disease". Can J
Ophthalmol. 42 (3): 425–
38. doi:10.3129/I07-044. PMID 17
508040.
59. Jump up^ Tsai JC, Song BJ, Wu
L, Forbes M (September 2007).
"Erythropoietin: a candidate
neuroprotective agent in the
treatment of glaucoma". J
Glaucoma. 16 (6): 567–
71. doi:10.1097/IJG.0b013e31815
6a556. PMID 17873720.
60. Jump up^ Mozaffarieh M,
Flammer J (November 2007). "Is
there more to glaucoma treatment
than lowering IOP?". Surv
Ophthalmol. 52 (Suppl 2): S174–
79. doi:10.1016/j.survophthal.200
7.08.013. PMID 17998043.
61. Jump up^ Online Mendelian
Inheritance in
Man (OMIM) Glaucoma,
Congenital: GLC3 Buphthalmos -
231300
62. Jump up^ Shingleton B, Tetz M,
Korber N (March 2008).
"Circumferential viscodilation and
tensioning of Schlemm's canal
(canaloplasty) with temporal clear
corneal phacoemulsification
cataract surgery for open-angle
glaucoma and visually significant
cataract: one-year results". J
Cataract Refract Surg. 34 (3):
433–40. doi:10.1016/j.jcrs.2007.1
1.029. PMID 18299068.
63. Jump up^ Lewis RA, von Wolff
K, Tetz M, et al. (July 2007).
"Canaloplasty: circumferential
viscodilation and tensioning of
Schlemm's canal using a flexible
microcatheter for the treatment of
open-angle glaucoma in adults:
interim clinical study analysis". J
Cataract Refract Surg. 33 (7):
1217–26. doi:10.1016/j.jcrs.2007.
03.051. PMID 17586378.
64. Jump up^ Dada T, Sharma R,
Sinha G, Angmo D, Temkar S
(2016). "Cyclodialysis-enhanced
trabeculectomy with triple Ologen
implantation". Eur J
Ophthalmol. 26 (1): 95–
7. doi:10.5301/ejo.5000633. PMI
D 26044372.
65. Jump up^ Yuan, F; Li, L; Chen;
Yan; Wang
(2015). "Biodegradable 3D-
Porous Collagen Matrix (Ologen)
Compared with Mitomycin C for
Treatment of Primary Open-Angle
Glaucoma: Results at 5
Years". Journal of
Ophthalmology. 2015 (637537):
1–7. doi:10.1155/2015/637537. P
MC 4452460  . PMID 26078875.
66. ^ Jump up to:a b Dada, Tanuj; Amit
S; Saptorshi M; Meenakshi G
(May 2013). "Combined
Subconjunctival and Subscleral
ologen Implant Insertion in
Trabeculectomy". Eye
(Lond.). 27 (7):
889. doi:10.1038/eye.2013.76. P
MC 3709396  . PMID 23640614.
67. Jump up^ Cillino, S; Casuccio A;
Di Pace F; Cagini C; Ferraro LL
(Mar 2016). "Biodegradable
collagen matrix implant versus
mitomycin-C in trabeculectomy:
five-year follow-up". BMC
Ophthalmol. 16 (24). doi:10.1186/
s12886-016-0198-0. PMC 477956
9  . PMID 26946419.
68. Jump up^ "Eyelights Newsletter:
About Glaucoma New
Zealand" (PDF).
Glaucoma.org. Archived (PDF) fro
m the original on 2015-01-13.
Retrieved 2014-02-20.
69. Jump up^ Molteno AC,
Polkinghorne PJ, Bowbyes JA
(November 1986). "The vicryl tie
technique for inserting a draining
implant in the treatment of
secondary glaucoma". Aust N Z J
Ophthalmol. 14 (4): 343–
54. doi:10.1111/j.1442-
9071.1986.tb00470.x. PMID 3814
422.
70. Jump up^ Lewis RA (Aug 2014).
"Ab interno approach to the
subconjunctival space using a
collagen glaucoma stent". J
Cataract Refract Surg. 40 (8):
1301–6. doi:10.1016/j.jcrs.2014.0
1.032. PMID 24943904.
71. Jump up^ "Xen Gel
Stent". AqueSys.
AqueSys. Archived from the
original on 29 June 2015.
Retrieved 27 June 2015.
72. Jump up^ "Advances in
Glaucoma Filtration Surgery".
Glaucoma Today. Archived from
the original on 29 June 2015.
Retrieved 27 June 2015.
73. Jump up^ Rosentreter, Andre;
Andre M. Schild; Sven Dinslage;
Thomas S. Dietlein (Jan 2011).
"Biodegradable implant for tissue
repair after glaucoma drainage
device surgery". J
Glaucoma. 21 (2): 76–
8. doi:10.1097/IJG.0b013e318202
7ab0. PMID 21278584.
74. Jump up^ Rosentreter, Andre;
Anne C. Mellein; Walter W.
Konen; Thomas S. Dietlein (Sep
2010). "Capsule excision and
ologenTM implantation for
revision after glaucoma drainage
device surgery". Graefes Arch
Clin Exp Ophthalmol. 248 (9):
1319–24. doi:10.1007/s00417-
010-1385-y. PMID 20405139.
75. Jump up^ Rosentreter, A;
Mellein AC; Konen WW; Dietlein
TS (2010). "Capsule excision and
ologenTM implantation for
revision after glaucoma drainage
device surgery". Graefes Arch
Clin Exp Ophthalmol. 248 (9):
1319–24. doi:10.1007/s00417-
010-1385-y. PMID 20405139.
76. Jump up^ Oana, Stirbu; Jorge
Vila (December 2012). Shaarawy,
Tarek, ed. "Tube Exposure
Repair". Journal of Current
Glaucoma Practice. 6 (3): 139–
142. doi:10.5005/jp-journals-
10008-1121. Archived from the
original on 2013-07-01.
77. Jump up^ Pardianto G, et al.
(2006). "Some difficulties on
Glaucoma". Mimbar Ilmiah
Oftalmologi Indonesia. 3: 49–50.
78. Jump up^ Chiselita, D. "Non-
penetrating deep sclerectomy
versus trabeculectomy in primary
open-angle glaucoma
surgery". US National Library of
Medicine. Archived from the
original on 6 September 2017.
Retrieved 22 August 2017.
79. Jump up^ Iqbal "Ike" K. Ahmed
(1 September 2005). "Making the
Case for Nonpenetrating
Surgery". Review of
Ophthamology. 12 (9). Archived
from the original on 11 October
2007.
80. Jump up^ Aptel, F; Dumas S;
Denis P (2009). "Ultrasound
biomicroscopy and optical
coherence tomography imaging of
filtering blebs after deep
sclerectomy with new collagen
implant". Eur J
Ophthalmol. 19 (2): 223–
30. PMID 19253238.
81. Jump up^ Matthew, SJ;
Sarkisian S; Nathan B; James MR
(2012). "Initial experience using a
collagen matrix implant (ologen)
as a wound modulator with
canaloplasty: 12 month results".
Ft. Lauderdale: ARVO Congress.
82. Jump up^ Anisimova SY,
Anisimova SI, Larionov EV
(2012). "Biological drainage –
Xenoplast in glaucoma surgery
(experimental and 10-year of
clinical follow-up)" (PDF).
Copenhagen: EGS
Congress. Archived (PDF) from
the original on 2013-10-17.
83. Jump up^ Heijl, Anders;
Bengtsson, Boel; Hyman, Leslie;
Leske, M. Cristina (Dec 2009).
"Natural History of Open-Angle
Glaucoma". Ophthalmology. 116 (
12): 2271–
76. doi:10.1016/j.ophtha.2009.06.
042. PMID 19854514.
84. Jump up^ "Glaucoma".
Coopereyecare.com. 2013-07-
25. Archived from the original on
2013-12-13. Retrieved 2014-02-
20.
85. Jump up^ "Death and DALY
estimates for 2004 by cause for
WHO Member States" (xls). World
Health Organization.
2004. Archived from the original
on 2012-01-27.
86. ^ Jump up to:a b c Quigley, H A;
Broman, AT (March 2006). "The
number of people with glaucoma
worldwide in 2010 and
2020". British Journal of
Ophthalmology. 90 (3): 262–
67. doi:10.1136/bjo.2005.081224. 
PMC 1856963  . PMID 16488940
.
87. Jump up^ Sommer, Alfred;
Tielsch, James M.; Katz, Joanne;
Quigley, Harry A.; Gottsch, John
D.; Javitt, Jonathan C.; Martone,
James F.; Royall, Richard M.;
Witt, Kathe A.; Ezrine, Sandi (Nov
14, 1991). "Racial Differences in
the Cause-Specific Prevalence of
Blindness in East Baltimore". New
England Journal of
Medicine. 325 (20): 1412–
17. doi:10.1056/NEJM199111143
252004. PMID 1922252.
88. Jump up^ "Glaucoma and
Marijuana use". National Eye
Institute. June 21,
2005. Archived from the original
on December 27, 2009.
89. Jump up^ Ramulu, Pradeep
(March 2009). "Glaucoma and
disability: which tasks are
affected, and at what stage of
disease?". Current Opinion in
Ophthalmology. 20 (2): 92–
98. doi:10.1097/ICU.0b013e3283
2401a9. PMC 2692230  . PMID 1
9240541.
90. Jump up^ Akbari, M.; Akbari, S.;
Pasquale, L. R. (February 2009).
"The Association of Primary
Open-angle Glaucoma With
Mortality: A Meta-analysis of
Observational Studies". Archives
of Ophthalmology. 127 (2): 204–
10. doi:10.1001/archophthalmol.2
008.571. PMID 19204241.
91. Jump up^ Richard Bannister:
Treatise of One Hundred and
Thirteen Diseases of the Eyes
and Eyelids. London 1622
92. Jump up^ Leffler CT, et al.
(2017). "Ophthalmology in North
America: Early Stories (1491-
1801)". Ophthalmology and Eye
Diseases. 9: 1–
51. doi:10.1177/11791721177219
02. PMC 5533269  . PMID 28804
247.
93. Jump up^ Daniel Albert and
Diane Edwards: The History of
Ophthalmologist. Cambridge,
Mass. 1996
94. Jump up^ Harper,
Douglas. "glaucoma". Online
Etymology Dictionary.
95. Jump up^ γλαύκωμα. Liddell,
Henry George; Scott, Robert; A
Greek–English Lexicon at
the Perseus Project.
96. Jump
up^ γλαυκός in Liddell and Scott.
97. Jump up^ Leffler CT, Schwartz
SG, Hadi TM, Salman A, Vasuki
V (2015). "The early history of
glaucoma: the glaucous eye (800
BC to 1050 AD)". Clinical
Ophthalmology. 9: 207–
15. doi:10.2147/OPTH.S77471. P
MC 4321651  . PMID 25673972. 
Archived from the original on
2015-02-26.
98. Jump up^ Sean K Wang, Robert
T Chang (2014). "An emerging
treatment option for glaucoma:
Rho kinase inhibitors". Clin
Ophthalmol. 8: 883–
89. doi:10.2147/OPTH.S41000. P
MC 4025933  . PMID 24872673.
99. ^ Jump up to:a b c Sena DF,
Lindsley K
(2017). "Neuroprotection for
treatment of glaucoma in
adults". Cochrane Database Syst
Rev. 1:
CD006539. doi:10.1002/1465185
8.CD006539.pub4. PMC 3478138
  . PMID 28122126.
100. Jump up^ "Marijuana
and Medicine: Assessing the
Science Base".
Nap.edu. Archived from the
original on 2014-02-25.
Retrieved 2014-02-20.
101. Jump up^ "Marijuana
and Medicine: Assessing the
Science Base (1999), Institute of
Medicine, National Academies
Press". Nap.edu. Archived from
the original on 2012-01-20.
Retrieved 2011-06-22.
102. ^ Jump up
to:a b "Complementary Therapy
Assessment: Marijuana in the
Treatment of Glaucoma".
American Academy of
Ophthalmology. Retrieved 2011-
05-04.
103. Jump
up^ "Complementary Therapy
Assessments : American
Academy of Ophthalmology".
One.aao.org. Retrieved 2011-01-
24.
104. Jump up^ Jampel,
Henry (2010). "American
Glaucoma Society Position
Statement: Marijuana and the
Treatment of Glaucoma". J
Glaucoma. 19 (2): 75.

External links[edit]
Classification V · T · D

ICD-10

ICD-9-

MeSH:

Disease

External resources Medlin

eMedic

 Glaucoma at Curlie (based


on DMOZ)
 GeneReview/NCBI/NIH/UW entry
on Primary Congenital Glaucoma
 Glaucoma, by Gary Heiting, OD
and Marilyn Haddrill, All About
Vision

[hide]

 Diseases of the human eye (H00–H59


 360–379)

[show]
Adnexa

[show]
Globe

[show]
Pathways

[show]
Infections
h85055227

21210-5

027278808

1935553n (data)

569850

529246
Categories: 
 Glaucoma
 Blindness
Navigation menu
 Not logged in

 Talk

 Contributions

 Create account

 Log in
 Article
 Talk
 Read
 Edit
 View history
Search
Go

 Main page
 Contents
 Featured content
 Current events
 Random article
 Donate to Wikipedia
 Wikipedia store
Interaction
 Help
 About Wikipedia
 Community portal
 Recent changes
 Contact page
Tools
 What links here
 Related changes
 Upload file
 Special pages
 Permanent link
 Page information
 Wikidata item
 Cite this page
Print/export
 Create a book
 Download as PDF
 Printable version
In other projects
 Wikimedia Commons
Languages
 ‫العربية‬
 Azərbaycanca
 বাংলা
 Беларуская
 Български
 Bosanski
 Català
 Čeština
 Dansk
 Deutsch
 Eesti
 Ελληνικά
 Español
 Esperanto
 Euskara
 ‫فارسی‬
 Français
 Gaeilge
 한국어
 Հայերեն
 हिन्दी
 Hrvatski
 Ido
 Bahasa Indonesia
 Íslenska
 Italiano
 ‫עברית‬
 ಕನ್ನಡ
 Қазақша
 Latina
 Latviešu
 Lietuvių
 Magyar
 Македонски
 മലയാളം
 मराठी
 Bahasa Melayu
 Nederlands
 नेपाली
 日本語
 Norsk
 ଓଡ଼ିଆ
 Oʻzbekcha/ўзбекча
 ਪੰ ਜਾਬੀ
 Papiamentu
 Piemontèis
 Polski
 Português
 Română
 Русский
 Simple English
 Slovenčina
 Slovenščina
 Српски / srpski
 Srpskohrvatski / српскохрватски
 Suomi
 Svenska
 தமிழ்
 Татарча/tatarça
 తెలుగు

 ไทย
 Türkçe
 Українська
 ‫اردو‬
 Tiếng Việt
 粵語
 中文
Edit links
 This page was last edited on 5 December 2017,

at 07:15.
 Text is available under the Creative Commons

Attribution-ShareAlike License; additional terms


may apply. By using this site, you agree to
the Terms of Use and Privacy Policy.
Wikipedia® is a registered trademark of
the Wikimedia Foundation, Inc., a non-profit
organization.

 Privacy policy
 About Wikipedia

 Disclaimers

 Contact Wikipedia

 Developers

 Cookie statement

 Mobile view

 Enable previews


 Product Profiles

 Rebates & Savings

 Find an Eye Doctor


Conjunctivitis: Bacterial, Viral, Allergic


And Other Types
By Marilyn Haddrill; contributions and review by Charles Slonim, MD

       Like This Page? Please Share!

On this page: Bacterial conjunctivitis • Viral conjunctivitis • Gonococcal and chlamydial


conjunctivitis• Neonatal conjunctivitis • Allergic conjunctivitis • Giant papillary conjunctivitis • Non-
infectious conjunctivitis

All forms of conjunctivitis — including bacterial, viral, allergic and other types — involve
inflammation of the transparent, mucous membrane (conjunctiva) covering the white part of the
eye or sclera.
Infectious causes of an inflamed eye and conjunctivitis include bacteria, viruses and fungi. Non-
infectious causes include allergies, foreign bodies and chemicals.
The phrase "pink eye" is commonly used to refer to conjunctivitis, because pinkness or redness
of the conjunctiva is one of the most noticeable symptoms.
Types Of Conjunctivitis

Bacterial conjunctivitis is a common type of pink eye, caused by bacteria that infect the eye
through various sources of contamination. The bacteria can be spread through contact with an
infected individual, exposure to contaminated surfaces or through other means such as sinus or
ear infections.

Allergic conjunctivitis can result when your eyes encounter a substance to which they are overly
sensitive, such as pollen in the air.

The most common types of bacteria that cause bacterial conjunctivitis include Staphylococcus
aureus, Haemophilus influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa.
Bacterial conjunctivitis usually produces a thick eye discharge or pus and can affect one or both
eyes.
As with any bacterial infection, antibiotics are required to eliminate the bacteria. Treatment of
bacterial conjunctivitis is typically accomplished with topical antibiotic eye drops and/or eye
ointments. The treatment usually takes from one to two weeks, depending on the severity of the
infection.
Viral conjunctivitis is another common type of pink eye that is highly contagious, because
airborne viruses can be spread through sneezing and coughing. Viral conjunctivitis also can
accompany common viral upper respiratory infections such as measles, the flu or the common
cold.
Viral conjunctivitis usually produces a watery discharge. Typically the infection starts in one eye
and quickly spreads to the other eye.
Unlike with bacterial infections, antibiotics will not work against viruses. No eye drops or
ointments are effective against the common viruses that cause viral conjunctivitis. But viral
conjunctivitis is self-limited, which means it will go away by itself after a short time.

TYPES OF PINK EYE

Typically with viral conjunctivitis, the third through the fifth days are the worst. After that, eyes
begin to improve on their own.

Treatment of viral conjunctivitis usually involves supportive therapies, such as eye drops, that
help reduce the symptoms: for example, vasoconstrictors to whiten the eye, decongestants to
reduce the surface swelling and antihistamines to reduce occasional itching. Treatments usually
are continued for one to two weeks, depending on the severity of the infection.
Gonococcal and chlamydial conjunctivitis are bacterial forms related to infections from
sexually transmitted diseases including gonorrhea and chlamydia. Newborn babies may be
exposed when they pass through the birth canal of an infected mother. Trachoma is a form of
chlamydial infection that causes scarring on the eye's surface. Trachoma is the world's leading
cause of preventable blindness.
Neonatal conjunctivitis found in newborn babies can cause blindness when left untreated. Up
to 10 percent of all pregnant women in the United States have a sexually transmitted chlamydial
infection. If these infections are untreated in mothers, the possibility that a newborn infant will
develop a related eye infection ranges from 10 percent to 20 percent.*

Save 10-30% off your eye exam using the BenefitsPal™ card

What is more important than your vision? Find local eye doctor to get an eye
exam

Another type of sexually transmitted disease related to the herpes simplex virus type 2 found in
the genital area can infect eyes of infants as they are born. Herpes simplex virus type 1, a
cause of cold sores on the mouth, also can cause a type of eye herpes that results in pink eye.
If you are pregnant and suspect you may have a sexually transmitted disease, you need to be
checked and possibly treated for any infection before the birth of your baby.

In the United States, an antibiotic ointment often is applied as a basic standard of care for
newborn infants, to help prevent the possibility of certain eye infections.
Allergic conjunctivitis caused by eye allergies is very common. Eye allergies, like other types,
can be triggered by allergens including pollen, animal dander and dust mites.
The most common symptom of allergic conjunctivitis is itchy eyes, which may be relieved with
special eye drops containing antihistamines to control allergic reactions. These eye drops are
available both over the counter and by prescription.
Avoiding the allergen is also important in the treatment of allergic conjunctivitis. Allergic
conjunctivitis can be seasonal or perennial (year-round), depending on the allergen causing the
reaction.

Giant papillary conjunctivitis (GPC) usually involves both eyes and often affects soft contact
lens wearers. This condition may cause contact lens intolerance, itching, a heavy discharge,
tearing and red bumps on the underside of the eyelids.
You'll need to stop wearing your contact lenses, at least for a little while. Your eye doctor may
also recommend that you switch to a different type of contact lens, to reduce the chance of the
conjunctivitis coming back.
For example, you might need to switch from soft contacts to gas permeable ones or vice versa.
Or you might need to try a type of lens that you replace more frequently, such as disposable
contact lenses. GPC can also result from artificial eyes (prosthetics), stitches and more. Your
eye doctor will decide if removal is appropriate.
Non-infectious conjunctivitis from eye irritation causing pink eye symptoms that can result
from many sources, including smoke, diesel exhaust, perfumes and certain chemicals. Some
forms of conjunctivitis also result from sensitivity to certain ingested substances, including herbs
such as eyebright and turmeric.**
Certain forms of pink eye, including giant papillary conjunctivitis, can be caused by the eye's
immune responses, such as a reaction to wearing contact lenses or ocular prosthetics (artificial
eyes). A reaction to preservatives in eye drops or ointments also can cause toxic
conjunctivitis. 

Back to top ⤴
Home » Conditions » Pink Eye » Types of Conjunctivitis
References & Notes >>

[Page updated September 2017]


More Pink Eye Articles
Conjunctivitis (Pink Eye) | Conjuntivitis (Spanish)
Conjunctivitis Treatment | Conjunctivitis Types
How Long Does Pink Eye Last? | How Long Is Pink Eye Contagious?
How to Get Rid of Pink Eye

       Like This Page? Please Share!

RECOMMENDED FOR YOU

 Get preservative-free relief. Try Clear Eyes Pure Relief® for Dry Eyes

 Questions about cataracts? Find all the answers in My Cataract Journey

 Dry and irritated eyes? The problem may be your eyelids

 Contact Lenses
o
 CONTACT LENSES
 Contact lens basics
 Daily contact lenses
 Understanding your contact lens Rx
 Contacts for astigmatism
 How to clean and disinfect soft contacts
 What's new in contact lenses
 Go to section for more topics »

 LASIK & Vision Surgery


o
 LASIK & VISION SURGERY
 Basics of corrective eye surgery
 Presbyopia surgery after age 40
 How LASIK works
 LASIK & PRK FAQ
 Why PRK is sometimes better than LASIK
 How to choose a great LASIK surgeon
 Go to section for more topics »

 Eyeglasses
o
 EYEGLASSES
 Frames for your personality
 Which frames would look best on you?
 10 tips for buying children's eyewear
 How to choose the best lenses for your needs
 How to read your eyeglasses prescription
 How to get thinner lenses
 Go to section for more topics »

 Sunglasses
o
 SUNGLASSES
 UV light & your eyes
 Today's AccuWeather UV index map
 Why do kids need sunglasses?
 Test your knowledge of sunglasses
 New sunglass trends
 Go to section for more topics »

 Eye Exams
o
 EYE EXAMS
 What to expect during the exam
 Eye charts and eye tests
 Online eye tests: What you need to know
 Color blindness test
 Visual acuity: Is 20/20 vision "perfect" vision?
 Go to section for more topics »

 Conditions A-Z
o
 EYE PROBLEMS - main page
 Conditions articles in Spanish
 Common eye disorders
 Eye symptoms A-Z
 Acanthamoeba keratitis
 Allergies of the eye
 Amblyopia / lazy eye
 Astigmatism
 Bell's palsy
 Bionic eyes
 Black eye
 Blepharitis
 Blurry vision
 Burning eyes
 Cataracts (28 articles)
 Cataract lenses / IOLs
 Chalazion
 Clinical trials - eye diseases
 CMV retinitis
 Color blindness
 Conjunctivitis / pink eye (6 articles)
 Conjuntivitis (Spanish version)
 Cornea transplant
 Corneal abrasion (scratched eye)
 Corneal crosslinking
 Corneal ulcer
 Crossed eyes (3 articles)
 Detached retina
 Diabetic retinopathy (5 articles)
 Different colored eyes (heterochromia)
 Double vision / diplopia
 Drooping eyelids
 Dry eye infographic - sponsored
 Dry eye treatment (plus 10 more articles)
 Eye color
 Eye color chart
 Eye discharge
 Eye drops: how to choose
 Eye exercises: do they work?
 Eye infections
 Eye injuries
 Eye injury prevention
 Eye occlusions / strokes
 Eye pain
 Eye twitching
 Floaters, spots, flashes


 Fuchs' corneal dystrophy
 Fungal keratitis eye infection
 Glaucoma (10 articles)
 Herpes of the eye
 Higher-order aberrations
 Hyperopia / farsightedness
 Hyphema
 Iritis
 Itchy eyes
 Keratoconus (5 articles)
 Keratoconus treatment - Intacs
 Legal blindness
 Macular degeneration (9 articles)
 Macular dystrophy
 Macular hole
 Meibomian gland dysfunction (MGD)
 Milia (tiny eyelid cysts)
 Myopia / nearsightedness
 New eye care products
 News about vision & the eyes
 Nystagmus
 Ocular herpes
 Ocular hypertension / high eye pressure
 Ocular migraine
 Ocular rosacea
 Optic neuritis
 Peripheral vision loss
 Photophobia / light sensitivity
 Pinguecula
 Pink eye (6 articles)
 Pollen count map
 Presbyopia
 Prosthetic eye / enucleation surgery
 Pterygium
 Ptosis / drooping eyelids
 Red eyes, bloodshot eyes
 Retinitis pigmentosa
 Sjogren's syndrome
 Snow blindness
 Stargardt's disease
 Strabismus (3 articles)
 Stye or sty
 Stye treatment
 Subconjunctival hemorrhage
 Swollen eyelids
 Uveitis
 Vitrectomy / vitreoretinal procedures

 Cataracts
o
 CATARACTS
 About cataract surgery
 About intraocular lenses / IOLs
 Multifocal IOLs
 How to choose a cataract surgeon
 Risks & complications
 Go to section for more topics »

 Dry Eyes
o
 DRY EYES
 About dry eye syndrome
 Answers from a dry eye expert
 Contact lenses for dry eyes
 Dry eye infographic - sponsored
 Flaxseed oil and fish oil for dry eyes
 Go to section for more topics »

 Low Vision
o
 LOW VISION
 Magnifiers - buyer's guide
 Finding a low vision doctor
 How to help someone with low vision
 Vision aids for distance viewing
 Go to section for more topics »

 Digital Eye Strain


o
 DIGITAL EYE STRAIN
 10 ways to relieve computer eye strain
 Blue light from digital devices: bad for eyes?
 Computer eyeglasses
 Children and computer vision syndrome
 7 things that give you eye strain at work
 Go to section for more topics »

 Sports Vision
o
 SPORTS VISION
 Contact lenses for sports
 Protective sports eyewear
 Choosing the right lens tint for your sport
 Eyeglasses for sports
 12 tips for buying ski goggles
 Go to section for more topics »

 Eye Safety
o
 EYE SAFETY
 Eye safety basics
 How to tell if an eye injury is serious
 Getting the right safety glasses
 [Video] How to prevent eye injuries
 Toys to avoid to keep kids' eyes safe
 Go to section for more topics »

 Nutrition & Eyes


o
 EYE NUTRITION
 Guide to nutrition for healthy eyes
 Vitamin A and beta-carotene facts
 Carotenoids - how they keep your eyes healthy
 Cataract prevention with nutrition
 Flaxseed oil vs. fish oil for dry eyes
 Go to section for more topics »

 Children's Vision
o
 CHILDREN'S VISION
 Infant vision
 Myopia control / cure
 8 warning signs of vision problems in kids
 Kids & computer vision syndrome
 Vision therapy for children
 Go to section for more topics »

 Teens
o
 TEENS
 5 tips for choosing eyeglasses
 Sunglasses - trends for teens
 Nutrition for your eyes
 Asking your parents for contacts? What to know
 Go to section for more topics »

 Vision Over 40
o
 VISION OVER 40
 Pros and cons of reading glasses
 Multifocal contact lenses
 Safety tips for improving night driving
 Combining options for presbyopia
 Go to section for more topics »
 Vision Over 60
o
 VISION OVER 60
 How vision changes as you age
 8 ways to protect your eyesight
 How good nutrition protects aging eyes
 Senior eye exams at no cost
 Safe driving after 60
 Go to section for more topics »

 Cosmetic Procedures
o
 COSMETIC EYE SURGERY
 Botox FAQ
 Eyelid surgery / blepharoplasty
 Latisse for eyelashes - is it safe?
 Puffy eyes & dark circles
 Go to section for more topics »

 Vision Insurance
o
 VISION INSURANCE
 How to choose a plan
 How to use vision insurance
 Glossary of vision insurance terms
 Medicare / Medicaid vision benefits
 VSP - how to make the most of your benefits
 Go to section for more topics »

 Resources
o
 RESOURCES
 Eye anatomy / parts of the eye
 Glossary of vision terms
 Buy smarter - Be a better eye care consumer
 How to put in eye drops
 Learn about these great vision charities
 Mobile apps for your eyes and vision
 Go to section for more topics »
AllAboutVision.com  All About Vision and
About  AllAboutVision.com are registered
Media Kit  trademarks of AAV Media, LLC. ©
Press Info  2000-2017 AAV Media, LLC.
Contact  This site complies with the
Site Map  All About Vision is a Supporter HONcode standard for
Terms of Use  National Sponsor of Optometry Giving trustworthy health
Privacy Policy Sight and we encourage our readers to information. Please click here to
support these humanitarian eye care verify.
organizations.

Follow Us 


Text and images on this website

are copyright protected and

reproduction is prohibited by law.

You may print or email pages for
personal use. Read our policy.

You might also like